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Aortic Valve Stenosis

Cardiovascular Medicine · NLM MeSH · updated 2026-10-29 · version 1

Citations verified against PubMedNot yet clinician-reviewed9 referencesApproximately 3 min read

A pathological constriction that can occur above (supravalvular stenosis), below (subvalvular stenosis), or at the aortic valve.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

Definition and research guide

This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.

Content available: 3 complete abstracts (550 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.

Definition

A pathological constriction that can occur above (supravalvular stenosis), below (subvalvular stenosis), or at the aortic valve. It is characterized by restricted outflow from the left ventricle into the aorta.

Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.

Also known as: Aortic Valve Stenoses; Stenoses, Aortic Valve; Stenosis, Aortic Valve; Valve Stenoses, Aortic; Valve Stenosis, Aortic; Aortic Stenosis; Stenoses, Aortic; Stenosis, Aortic.

Where it fits in the MeSH classification

Broader topics
Aortic Valve Disease; Ventricular Outflow Obstruction
Narrower topics
Aortic Stenosis, Subvalvular; Aortic Stenosis, Supravalvular
See also
Cardiomyopathy, Hypertrophic

Related concepts

  • Aortic Valve
  • Left Ventricle
  • Aorta

Research landscape

PubMed indexes 58,051 records tagged with the MeSH heading “Aortic Valve Stenosis” (counts retrieved 2026-10-29). 15,958 of them (27.5%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 18,465 records.

Reviews account for 6,803 records (11.7%) and meta-analyses for 948. Randomized controlled trials number 856 (1.5%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.

PubMed records by publication periodthrough 1999: 15,485 records; 2000-2009: 8,143 records; 2010-2019: 18,465 records; 2020 onward: 15,958 records15,485through 19998,1432000-200918,4652010-201915,9582020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 199915,485
2000-20098,143
2010-201918,465
2020 onward15,958
Share of records by publication typeReviews: 11.7 percent; Meta-analyses: 1.6 percent; Randomized controlled trials: 1.5 percentReviews11.7% (6,803)Meta-analyses1.6% (948)Randomized controlled trials1.5% (856)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 58,051 PubMed records
TypeRecordsShare
Reviews6,80311.7%
Meta-analyses9481.6%
Randomized controlled trials8561.5%

Method: PubMed query "Aortic Valve Stenosis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.

Reading the evidence in cardiovascular medicine

Cardiovascular medicine has an unusually large body of randomized trials, so the type of outcome matters: hard clinical events such as death, heart attack and stroke carry more weight than changes in blood pressure, cholesterol or imaging markers that only predict risk. Observational studies can show associations but are confounded by age, lifestyle and other illness. Check whether a result is about prevention or treatment, the baseline risk of participants, and the absolute rather than only the relative size of any benefit.

Evidence from open-access studies

These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.

Study comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Calcific Aortic Valve Disease: Mechanism and Future Therapeutic Strategies
Hwang G, Jo S, Kwon H, Kwon M, Ku I, Song JK, et al.
2026Review article
Design not recorded in structured metadata
2cc by
PMID 41892332 · DOI · PMC13024875
Evolving strategies in obstructive hypertrophic cardiomyopathy: myosin inhibitors as monotherapy compared with beta-blockers
Grupper A, Sverdlov AL, Cheema BS, Nasrollahizadeh A, Hosseini K
2026Review article
Design not recorded in structured metadata
2cc by
PMID 41848906 · DOI · PMC12999815
Probing relaxed myosin states in hypertrophic cardiomyopathy by second harmonic-generation microscopy
Arecchi G, Dente M, Ma W, Scellini B, Piroddi N, Scardigli M, et al.
2026Research article
Design not recorded in structured metadata
2cc by
PMID 42606952 · DOI · PMC13480991

Calcific Aortic Valve Disease: Mechanism and Future Therapeutic Strategies [1]

Review article Hwang G, Jo S, Kwon H, Kwon M, Ku I, Song JK, et al. · · 2026 · cited 2 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Calcific aortic valve disease (CAVD) is an active pathological process driven by complex cellular and molecular mechanisms rather than passive aging.
Closing excerpt
A deeper understanding of CAVD pathophysiology may facilitate the development of targeted therapies to delay or prevent disease progression.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (188 words)

Calcific aortic valve disease (CAVD) is an active pathological process driven by complex cellular and molecular mechanisms rather than passive aging. The disease is characterized by endothelial dysfunction, lipid infiltration, inflammation, extracellular matrix remodeling, and osteogenic differentiation of valvular interstitial cells, ultimately leading to hydroxyapatite deposition and progressive valve calcification. Key signaling pathways, including Notch, Wnt/β-catenin, BMP2, and TGF-β, play critical roles in osteogenic reprogramming, while inflammatory cytokines such as IL-6, IL-1β, and TNF-α contribute to a pro-calcific microenvironment. To summarize current knowledge on CAVD pathophysiology and emerging therapeutic strategies, relevant preclinical studies were identified through searches of PubMed, and clinical trials were identified through ClinicalTrials.gov. Evidence indicates that extracellular matrix remodeling, fibrosis, and dysregulated phosphate metabolism, particularly involving TNAP and DPP-4, further accelerate disease progression. Despite advances in understanding disease mechanisms, effective pharmacological therapies remain limited, with the current treatment largely restricted to valve replacement. Emerging therapeutic approaches targeting molecular pathways, including enzyme inhibition, RNA-based therapeutics, and advanced drug delivery systems, may offer promising strategies for disease modification. A deeper understanding of CAVD pathophysiology may facilitate the development of targeted therapies to delay or prevent disease progression.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41892332 · DOI · PMC13024875

Evolving strategies in obstructive hypertrophic cardiomyopathy: myosin inhibitors as monotherapy compared with beta-blockers [2]

Review article Grupper A, Sverdlov AL, Cheema BS, Nasrollahizadeh A, Hosseini K · · 2026 · cited 2 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Obstructive hypertrophic cardiomyopathy (oHCM) is characterized by asymmetric hypertrophy, left ventricular outflow tract (LVOT) obstruction, and impaired diastolic function.
Closing excerpt
BBs remain clinically relevant for specific patient subgroups, but the advent of CMIs marks a paradigm shift from symptomatic relief toward targeted disease modification in oHCM.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (195 words)

Obstructive hypertrophic cardiomyopathy (oHCM) is characterized by asymmetric hypertrophy, left ventricular outflow tract (LVOT) obstruction, and impaired diastolic function. β-adrenergic blockers (BB) have long been the cornerstone of medical therapy, providing symptomatic improvement but without disease-modifying effects. Cardiac myosin inhibitors (CMIs), including mavacamten and aficamten, represent a new therapeutic class targeting the hypercontractile sarcomere. Randomized trials have demonstrated substantial reductions in LVOT gradients and improvements in exercise capacity, New York Heart Association functional class, and quality of life, with an acceptable safety profile. Subgroup analyses from EXPLORER-HCM and FOREST-HCM suggested that concomitant BB therapy may blunt the exercise capacity benefits of CMIs. The MAPLE-HCM trial provided the first direct head-to-head comparison, showing that aficamten monotherapy was superior to metoprolol in improving peak oxygen uptake, functional status, and hemodynamic parameters. Current evidence indicates that CMIs offer greater efficacy than BB in improving exercise tolerance and LVOT obstruction in oHCM, supporting their role as potential first-line therapy. However, long-term safety, durability of benefit, optimal sequencing, and patient selection require further study. BBs remain clinically relevant for specific patient subgroups, but the advent of CMIs marks a paradigm shift from symptomatic relief toward targeted disease modification in oHCM.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41848906 · DOI · PMC12999815

Probing relaxed myosin states in hypertrophic cardiomyopathy by second harmonic-generation microscopy [3]

Research article Arecchi G, Dente M, Ma W, Scellini B, Piroddi N, Scardigli M, et al. · · 2026 · cited 2 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
This study explores the use of polarized second-harmonic generation (pSHG) to investigate myosin conformation in the relaxed state, differentiating between the actin-available, disordered (ON) state and the energy-conserving, ordered (OFF) state.
Closing excerpt
ATPase assays reveal increased resting ATPase activity in R403Q samples, which persists even in the presence of 2-deoxyATP, suggesting that the elevated energy consumption in the R403Q mutation is driven by both a population shift toward the ON state and enhanced myosin ATPase activity per motor head.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (167 words)

This study explores the use of polarized second-harmonic generation (pSHG) to investigate myosin conformation in the relaxed state, differentiating between the actin-available, disordered (ON) state and the energy-conserving, ordered (OFF) state. By shifting the ON/OFF equilibrium using both physical and chemical manipulations, we demonstrate the sensitivity of pSHG in quantifying the ON/OFF ratio in skeletal and cardiac tissues. Comparisons with X-ray diffraction measurements further validate our findings. Applying this approach to a sarcomeric mutation associated with hypertrophic cardiomyopathy, we show that R403Q/MYH7-mutated minipig ventricle tissue exhibits a higher ON fraction compared to controls. This difference is abolished under high concentrations of a myosin activator (2-deoxyATP) and an inhibitor (Mavacamten), indicating structural similarity between R403Q and controls in these two states. ATPase assays reveal increased resting ATPase activity in R403Q samples, which persists even in the presence of 2-deoxyATP, suggesting that the elevated energy consumption in the R403Q mutation is driven by both a population shift toward the ON state and enhanced myosin ATPase activity per motor head.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42606952 · DOI · PMC13480991

Key reviews and meta-analyses

The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.

  • Research article Shared genetic pathways contribute to risk of hypertrophic and dilated cardiomyopathies with opposite directions of effect [4]
    Tadros R, Francis C, Xu X, Vermeer AMC, Harper AR, Huurman R, et al. · Nat Genet · 2021 · cited 247 times (Europe PMC)
  • Research article Subclinical Leaflet Thrombosis After Transcatheter Aortic Valve Replacement: A Meta-Analysis [5]
    Bogyi M, Schernthaner RE, Loewe C, Gager GM, Dizdarevic AM, Kronberger C, et al. · JACC Cardiovasc Interv · 2021 · cited 106 times (Europe PMC)
  • Research article Dyslipidemia, inflammation, calcification, and adiposity in aortic stenosis: a genome-wide study [6]
    Yu Chen H, Dina C, Small AM, Shaffer CM, Levinson RT, Helgadóttir A, et al. · Eur Heart J · 2023 · cited 103 times (Europe PMC)
  • Research article Meta-Analysis of Penetrance and Systematic Review on Transition to Disease in Genetic Hypertrophic Cardiomyopathy [7]
    Topriceanu CC, Pereira AC, Moon JC, Captur G, Ho CY · Circulation · 2024 · cited 75 times (Europe PMC)
  • Research article Transcatheter versus surgical aortic valve replacement in lower-risk and higher-risk patients: a meta-analysis of randomized trials [8]
    Ahmad Y, Howard JP, Arnold AD, Madhavan MV, Cook CM, Alu M, et al. · Eur Heart J · 2023 · cited 74 times (Europe PMC)
  • Research article Outcomes After Transcatheter Aortic Valve Replacement in Bicuspid Versus Tricuspid Anatomy: A Systematic Review and Meta-Analysis [9]
    Montalto C, Sticchi A, Crimi G, Laricchia A, Khokhar AA, Giannini F, et al. · JACC Cardiovasc Interv · 2021 · cited 73 times (Europe PMC)

References

  1. Hwang G, Jo S, Kwon H, Kwon M, Ku I, Song JK, et al.. Calcific Aortic Valve Disease: Mechanism and Future Therapeutic Strategies. . 2026. PMID 41892332 · DOI · PMC13024875
  2. Grupper A, Sverdlov AL, Cheema BS, Nasrollahizadeh A, Hosseini K. Evolving strategies in obstructive hypertrophic cardiomyopathy: myosin inhibitors as monotherapy compared with beta-blockers. . 2026. PMID 41848906 · DOI · PMC12999815
  3. Arecchi G, Dente M, Ma W, Scellini B, Piroddi N, Scardigli M, et al.. Probing relaxed myosin states in hypertrophic cardiomyopathy by second harmonic-generation microscopy. . 2026. PMID 42606952 · DOI · PMC13480991
  4. Tadros R, Francis C, Xu X, Vermeer AMC, Harper AR, Huurman R, et al.. Shared genetic pathways contribute to risk of hypertrophic and dilated cardiomyopathies with opposite directions of effect. Nat Genet. 2021. PMID 33495596 · DOI · PMC7611259
  5. Bogyi M, Schernthaner RE, Loewe C, Gager GM, Dizdarevic AM, Kronberger C, et al.. Subclinical Leaflet Thrombosis After Transcatheter Aortic Valve Replacement: A Meta-Analysis. JACC Cardiovasc Interv. 2021. PMID 34949391 · DOI
  6. Yu Chen H, Dina C, Small AM, Shaffer CM, Levinson RT, Helgadóttir A, et al.. Dyslipidemia, inflammation, calcification, and adiposity in aortic stenosis: a genome-wide study. Eur Heart J. 2023. PMID 37038246 · DOI · PMC10232274
  7. Topriceanu CC, Pereira AC, Moon JC, Captur G, Ho CY. Meta-Analysis of Penetrance and Systematic Review on Transition to Disease in Genetic Hypertrophic Cardiomyopathy. Circulation. 2024. PMID 37929589 · DOI · PMC10775968
  8. Ahmad Y, Howard JP, Arnold AD, Madhavan MV, Cook CM, Alu M, et al.. Transcatheter versus surgical aortic valve replacement in lower-risk and higher-risk patients: a meta-analysis of randomized trials. Eur Heart J. 2023. PMID 36660821 · DOI
  9. Montalto C, Sticchi A, Crimi G, Laricchia A, Khokhar AA, Giannini F, et al.. Outcomes After Transcatheter Aortic Valve Replacement in Bicuspid Versus Tricuspid Anatomy: A Systematic Review and Meta-Analysis. JACC Cardiovasc Interv. 2021. PMID 34620393 · DOI

About this article

Sources
NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
Verification
Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
Review state
automated source verified; no human expert review has been recorded yet.
Version
1, last updated 2026-10-29.

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At a glance

58,051
PubMed records on this heading
27%
published since 2020
6,803
review articles
856
randomized trials
9
verified references below

Counts come from PubMed on 2026-10-29; they show how much has been written, not how strong the evidence is.

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  • Mitral Valve ProlapseCardiovascular Medicine
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  • Aortic RuptureCardiovascular Medicine

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